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Wilson Liao, MD

Background: Psoriasis is a common cutaneous and systemic inflammatory disease that represents a fascinating intersection between genetics, immunology, microbiology, and metabolism. Over forty genetic loci contributing to psoriasis susceptibility have been identified. The affected genes result in abnormal responses of both the innate and adaptive immune system, influencing diverse cell types such as keratinocytes, T cells, dendritic cells, NK cells, and macrophages. Psoriasis may be triggered by a number of bacterial and viral infections and it is likely that psoriasis is influenced by microbiota residing on the skin and in the gut. Patients with psoriasis have systemic inflammation leading to increased risk of heart attack, stroke, type 2 diabetes, metabolic syndrome, and other autoimmune diseases. Due to the accessibility of skin for sampling, psoriasis represents an attractive model system to study multiple facets of human biology. The Liao laboratory utilizes a translational approach in which patient data and biosamples from the clinic are directly studied in the laboratory.

Identification of novel psoriasis genes. We use genome-wide association data, exome and whole genome sequencing data, and functional mapping methods to identify both common and rare susceptibility variants in psoriasis.

Role of diet and microbiome. We combine epidemiologic surveys of diet with microbial profiling of the skin and gut in psoriasis to explore the role of these factors in modulating psoriasis severity, systemic inflammation, and associated co-morbidities.

Autoimmune disease and HIV-1 control. Our lab has identified a link between the genetic determinants of autoimmune disease (psoriasis, Crohn’s) and immunologic control of HIV-1 replication. Evolutionarily, beneficial adaptation leading to heightened immune responses against retroviruses may have detrimentally increased risk of autoimmune disease. We are exploring how the genetic and immunologic features of psoriasis relate to an antiviral state.